Autophagy modulation for cancer therapy

Zhineng J. Yang, Cheng E. Chee, Shengbing Huang, Frank A. Sinicrope

Research output: Contribution to journalReview article

105 Scopus citations

Abstract

Autophagy is a homeostatic and catabolic process that enables the sequestration and lysosomal degradation of cytoplasmic organelles and proteins that is important for the maintenance of genomic stability and cell survival. Beclin 1+/-gene knockout mice are tumor prone, indicating a tumor suppressor role for autophagy. Autophagy is also a mechanism of stress tolerance that maintains cell viability and can lead to tumor dormancy, progression and therapeutic resistance. Many anticancer drugs induce cytotoxic stress that can activate pro-survival autophagy. In some contexts, excessive or prolonged autophagy can lead to tumor cell death. Inhibition of cytoprotective autophagy by genetic or pharmacological means has been shown to enhance anticancer drug-induced cell death, suggesting a novel therapeutic strategy. Studies are ongoing to define optimal strategies to modulate autophagy for cancer prevention and therapy, and to exploit it as a target for anticancer drug discovery.

Original languageEnglish (US)
Pages (from-to)169-176
Number of pages8
JournalCancer Biology and Therapy
Volume11
Issue number2
DOIs
StatePublished - Jan 15 2011

Keywords

  • Autophagy
  • Beclin 1
  • Cancer treatment
  • Cell death

ASJC Scopus subject areas

  • Molecular Medicine
  • Oncology
  • Pharmacology
  • Cancer Research

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